Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Patho II > GI > Flashcards

GI Flashcards

1
Q

Abscess

A

A localized pocket of infection or purulent exudate surrounded by inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Adhesion

A

A band of fibrous scar tissue forming an abnormal connection between two surfaces or structures (binding two loops of intestine together)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Autodigestion

A

Abnormal destruction of tissues by activated digestive enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Bolus

A

A round mass of food ready to be swallowed; a dose of concentrated drug administered intravenously all at once

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Calculi

A

A stone developing in the body (kidney or bile)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Cholestasis

A

Obstructed flow of bile in the liver or biliary tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Chyme

A

Thick, semifluid mixture of partially digested food passing out of the stomach into the duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Colostomy

A

Surgical creation of an artificial opening from the colon onto the abdominal surface

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Exocrine

A

a

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Fecalith

A

a hard mass of feces, often impacted, in the intestine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Gastrectomy

A

A surgical procedure where all, or a portion of the stomach is removed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Gluconeogenesis

A

The production of glucose from protein or fat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Glycogen

A

A polysaccharide, made up of glucose molecules, stored in skeletal muscle or the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Hematemesis

A

Vomiting blood; may be called “coffee-grounds” vomitus because it appears brown and granular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Hepatocytes

A

Epithelial cell of liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Hepatotoxins

A

A substance that damages the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Hyperbilirubinemia

A

a

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Icterus

A

Jaundice

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Ileostomy

A

A surgical procedure where the ileum (small intestine) is attached to the abdominal wall to a bag outside the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Impaction

A

An immovable packing such as food or feces in the intestines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Mastication

A

The process of chewing food in preparation for swallowing and digesting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Melena

A

Black, tarry stool caused by bleeding in the digestive tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Mesentery

A

A double layer or peritoneum that supports the intestines and conveys blood vessels and nerves to supply the wall of the intestine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Multiparity

A

a

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Occult

A

Hidden, difficult to detect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Pruritus

A

Itching sensation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Retroperitoneal

A

Behind the peritoneal membrane against the abdominal wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Rugae

A

Characteristic folds of the gastric mucosa, especially evident when the stomach is contracted

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Sinusoids

A

a

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Splenomegaly

A

Enlarged spleen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Steatorrhea

A

Fatty, bulky stool resulting from malabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Stricture

A

Abnormal narrowing of a duct or tube

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Tenesmus

A

Spams or straining associated with forced or painful elimination of urine or stool

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Ulcerogenic

A

Producing or aggravating ulcers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Gastroenteritis

A

Inflammatory process caused by infection or allergic reactions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Intestinal obstruction

A

Refers to a lack of movement of the intestinal contents through the intestine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Small intestine

A

20 feet long, 1 inch in diameter
Hangs in coils
Digests food
Has 3 regions (duodenum, jejunum, ileum)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Large Intestine

A

Begins at ileocecal valve, terminates at the anus
5 ft long
Nutrients absorbed and indigestible materials eliminated
Parts: Cecum, ascending, transverse, descending (sigmoid colon, rectum)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Simple Obstruction

A

Intussusception - telescoping of a section of bowel inside an adjacent section
Volvulus - twisting of section of intestine
Adhesions of tumours
Gradual obstructions from chronic inflammatory conditions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Intestinal Obstruction: Signs and Symptoms Simple Obstruction; Small Intestine

A

Vomiting and abdominal distention occur quickly
No stool or gas is passed
Restlessness and diaphoresis (septic; early sign of shock)
Tachycardia (early sign of shock)
Severe colicky abd. pain
Abdominal distention
Vomiting
Borborygmi - hyperactive rumbling by movement of gas in intestine
Intestinal rushes - intestinal muscle contracts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Intestinal Obstruction: Signs and Symptoms Simple Obstruction; Large Intestine

A

Obstructions develop slowly and with mild signs
Constipation and mild lower abd. pain
Abd. distention, anorexia and eventually vomiting with severe pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Functional obstruction or paralytic ileus

A

Peristalsis ceases due to neurologic impairment (spinal cord injury)
Distention of intestine occurs as fluids and electrolytes accumulate
Reflex spasms of the intestinal muscle do not occur
Remainder of process similar to mechanical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Etiology: Functional Obstruction

A

Inflammation related to severe schema
Pancreatitis, peritonitis, or infection in abd.
Hypokalemia, mesenteric thrombosis or toxemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Signs and Symptoms: Functional Obstruction

A

Bowel sounds decrease or are absent

Pain is steady

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Diagnostic Tests

A

Abdominal x-rays (presence of gas and fluid in intestine)
Barium enema - locating obstructions (allows us to visualize what is happening; not used if perforation is suspected)
If location unknown - lower GI tract study first then upper GI
Sigmoidoscopy or colonoscopy
CBC (infection, “cold sepsis”, clotting factors)
Electrolytes (K+, Na+)
Stool OB (3 tests over 3 days)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Colorectal Cancer: Pathophysiology

A

Begin as benign polyps
Grows undetected in the colon or rectum
Occurs in lower intestine
50+, sedentary lifestyles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Colorectal Cancer: Risk Factors

A

Familial risk
Long-term ulcerative colitis
Genetic factors
Environmental factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Colon Cancer: Pathophysiology

A

Direct extension into the bowel wall
Spread to neighbouring organs
Seed other organs
Metastasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Colon Cancer: Manifestations

A

Bleeding with BM (rectal cancers)
Change in bowel habits
Pain (goes away when peristalsis stops), anorexia, weight loss (feel full; not eating)
Prognosis depends on extent of the disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Colon Cancer: Complications

A 
Bowel obstruction (presenting symptom)
Perforation into neighbouring organs (stomach/bladder; will have darker, cloudy, foul, purulent, severe UTI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Colon Cancer; differences

A 
Transverse colon (15%); pain, obstruction, change in bowel habits, anemia
Descending colon (15%); pain, change in bowel habits, bright red blood in stool (no time for it to absorb before it leaves the body)
Rectum (45%); blood in stool, change in bowel habits (may have to go more frequently), rectal discomfort (severe, spasmodic)
Ascending colon (25%); pain, mass change in bowel habits, anemia (blood is not obvious, will see occult)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Crohn’s Disease

A

Inflammatory disorder
Genetic factor
Many similarities to other IBD (irritable bowel disease)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Crohn’s Pahophysiology

A 
Inflammatory lesions of bowel mucosa, ulcers and deep fissures develop (corrosion into the bowel)
Fistula formation
Skip lesions (definitive sign of crown's)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Crohn’s Manifestations

A

Diarrhea (perfuse, watery)
Abdominal pain, palpable mass
Lesions of the rectum, anus
Exacerbations and remissions (can be very controlled or very uncontrolled)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Crohn’s Complications

A 
Intestinal obstruction
Increased risk of cancer in the small intestine or colon
Adhesions (huge risk; lead to obstruction)
Abscess
Fistula formation (common in bladder)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Ulcerative Colitis

A

Inflammation fo rectum and progresses through colon (only regulated to lower GI)
Mucosa and submucosa inflamed
Tissue edematous and bleeds
Ulcerations develop
Bowel wall thicken and shorter (exacerbation and remission)
Attempts to heal - granulation tissue forms but is vascular and fragile; bleeds easily (anemic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

UC: Manifestations

A

Intermittent rectal bleeding and mucous
Urgency & cramping pain LLQ relieved by defecation
Anorexia, weight loss, anemia, fatigue associated with malabsorption and malnutrition - VB12, bile salts
Children - delayed growth and sexual maturation
Tenesmus - straining, persistent ineffective spasms rectum

58
Q

UC: Complications

A 
Perforated colon ( ^ risk)
Toxic megacolon (only treatment is to remove)
High risk for colon cancer
Anklosing spondylitis
Arthritis
Nephrolithiasis
59
Q

Crohn’s & UC: Diagnostics

A

Stool specimen - blood and mucus
Hematology
Chemistry - Albumin, Vitamins - nutritional status
Upper GI with small bowel follow through
Barium enema
Sigmoidoscopy or colonoscopy - visualize and biopsy

60
Q

Malabsorption: Pathophysiology

A

Celiac disease (can’t break down wheat; blood test to see if they lack the enzyme)
Lactose intolerance (can’t break down sugar)
Bowel resection
Short Bowel syndrome

61
Q

Malabsorption: Manifestations

A

Depends on the cause

62
Q

Celiac Disease: Diagnostic Tools

A

Stool samples
Blood tests
Intestinal biospy (confirms)

63
Q

Celiac Disease: Pathophysiology

A

Glutenteropathy
Malabsorption syndrome
Genetic defect in intestinal enzymes that prevent digestion of gliadin and breakdown gluten
Occurs in childhood and middle age

64
Q

Celiac Disease: Manifestations

A 
Infant 4-6 months
Streatorrhea (a condition that is characterized by chronic fatty diarrhea)
Muscle wasting
Failure to gain weight
Irratibility and malaise
Skin rash
65
Q

Dental Disorders

A

Caries (cavities)
Periodontal disease (general term)
Gingivitis (inflammation of gums)
Peridontitis (permanent loss)

66
Q

Dysphagia

A

Neurological deficit
Mechanical deficit
Muscular disorder
Mechanical obstruction

67
Q

Hiatal Hernia

A

Is a herniation of the stomach into the esophagus through an opening in the diaphragm

68
Q

Hiatal Hernia: Sliding

A

Stomach slides into thoracic cavity when supine and goes back when upright

69
Q

Hiatal Hernia: Paresophageal or rolling

A

Fundus and greater curvature causes stomach to roll up through the diaphragm

70
Q

Hiatal Hernia: Etiology and Pathophysiology

A

Multiple factors cause:
Weakening of the muscles in the diaphragm
Increased intra-abdominal pressure (pregnancy, obesity, ascites, poor nutrition, pts that are supine)

71
Q

Hiatal Hernia: Manifestations

A

Similar symptoms to GERD
Heartburn, especially after a meal (fat triggers acid reflux)
Dysphagia
Reflux and discomfort are associated with position

72
Q

Hiatal Hernia: Complications

A

GERD
Hemorrhage from erosion
Stenosis of the esophagus (^ risk for esophageal cancer)
Ulcerations of the herniated portion of the stomach
Strangulation of the hernia (Ischemia can occur if stomach is pushed up enough)
Regurgitation with tracheal aspiration

73
Q

Hiatal Hernia: Diagnostic

A

Barium swallow

Endoscopic examination

74
Q

Peptic Ulcer Disease

A

Condition characterized by erosion of GI mucosa resulting from digestive action of HCl and pepsin
Can be superficial or deep

75
Q

Peptic Ulcer Development

A

Lower esophagus
Stomach
Duodenum
10% of the population of Western countries suffers a duodenal or gastric ulcer during their lifetime

76
Q

Duodenum Ulcers

A

Occur at any age and in anyone
Increase risk between ages of 35-45
Account for 80% of all peptic ulcers
Associated with ^ HCl acid secretion

77
Q

Psychological Stress Ulcers

A

Acute ulcers that develop following a major physiological insult, such as trauma or surgery
A form of erosive gastritis

78
Q

Psychological Stress Ulcers: Complications

A

Hemorrhage
Perforation
Gastric outlet obstruction (an emergency, requires surgery)

79
Q

Appendicitis

A

Inflammation and infection of vermiform appendix
Most common reason for abdominal surgery
Most often seen in adolescents and young adults
Slightly higher incidence in males

80
Q

Appendicitis: Causes

A

Obstruction from fecalith (feces), gallstone, or foreign material
Obstruction due to twisting and kinking

81
Q

Stage 1: Simple Appendicitis

A 
Appendix is inflamed but intact
Manifestations
Generalized periumbilical pain
N&V
Low grade fever
82
Q

Stage 2: Gangrenous Appendicitis

A 
Tissue is necrotic and has microscopic perforations
Manifestations
Pain becomes more localized in RLQ
Rebound tenderness in McBurney's point
Positive Rosving's sign
83
Q

Stage 3: Perforated Appendix

A

Appendix ruptures and contens contaminate peritoneal cavity

Can occur within 24 hours

84
Q

Stage 3: Manifestations

A 
Pain briefly subsides with rupture then becomes more severe across abdomen as peritonitis (medical emergency) develops:
Abdomen is rigid
HR increases
Rapid, shallow breathing
Increased temp
Bowel sounds decrease
N&V
85
Q

Appendicitis: Diagnostic Tests

A

Diagnosis based on complete physical exam and CBC
WBC will be elevated
Ultrasound may be done to confirm diagnosis

86
Q

Peritonitis

A

Inflammation of peritoneal membranes
Result of chemical irritation or bacterial invasion
Chemical if not removed quickly, ultimately leads to bacterial peritonitis

87
Q

Peritonitis: Pathophysiology

A

Initially: Local inflammation of peritoneum and momentum produce thick sticky exudate
Temporarily seals the area
Occasionally inflammation subsides and abscess forms
Peristalsis may reduce in this area
If cause not removed inflammation/infection will spread

88
Q

Peritonitis

A 
Hypovolemic shock due to third-spacing
Fluid becomes purulent
Complications:
Obstruction - paralytic ileus
Septicemia - circulating toxins
89
Q

Peritonitis: Etiology

A

Abd. surgery - if foreign material remains or infection develops
Pelvic inflammatory disease - infection ascends uterus and fallopian tubes to peritoneal cavity

90
Q

Peritonitis: S&S

A

Sudden, severe, generalized abd. pain. Pain increases with movement
Localized pain at area of problem
Breathing restricted
V
Signs of dehydration and hypovolemia - dec. turgor, dry mucous membranes, pallor, low BP
Fever and leukocytosis - inflammation & infection
Abd. distention - rigid abd. signals involvement of parietal peritoneum
Dec. bowel sounds - paralytic ileum and secondary obstruction

91
Q

Peritonitis: Diagnostic Tests

A

Abd. x-ray - edematous and gaseous distention
Chest x-ray - elevated diaphragm
CBC - increase WBC
Paracentesis reveals bacteria, exudate, blood, pus or urine in abd.

92
Q

Jaundice

A

Also known as icterus
Hyperbilirubinemia
Refers to yellowish colour of skin and other tissues

93
Q

Jaundice

A

Disorders that cause jaundice are classified in 3 groups:

  • Prehepatic (before liver)
  • Intrahepatic (inside/ from the liver)
  • Posthepatic (outside the liver)
94
Q

Jaundice: Prehepatic

A

Results from excessive destruction of RBC
Characteristic of hemolytic anemias or transfusion reactions
Liver function normal but unable to handle the additional bilirubin
Physiologic jaundice of newborns - inc. hemolysis of RBC combined with immature liver

95
Q

Jaundice: Intrahepatic

A

Occurs in individuals with liver disease
Hepatitis or cirrhosis
Impaired uptake of bilirubin from blood and dec. conjugation of bilirubin by hepatocytes

96
Q

Jaundice: Posthepatic

A 
Caused by obstruction of bile flow into gallbladder or duodenum and backup in blood
Congenital atresia (absence of opening) of bile-ducts, obstruction caused by cholelithiasis, inflammation of liver or tumours
97
Q

Jaundice: Manifestations

A

Yellow sclera and skin
Changes in stool
Urine colour

98
Q

Jaundice: Diagnostic tests

A

Prehepatic - serum levels unconjugated bilirubin (indirect-acting) elevated
Posthepatic - results from inc. of conjugated bilirubin (direct)

99
Q

Hepatitis

A

Viral - A, B, C, D, E
Toxic or nonviral
Chronic noninfectious

100
Q

Hepatitis: May result from

A

Local infection (viral hepatitis)
Infection elsewhere in body (infectious, mononucleosis or amebiasis)
Chemical or drug toxicity

101
Q

Viral Hepatitis

A

Results from infection by a group of viruses that specifically target the hepatocytes

  • Hep. A Virus (HAV); common in foods
  • Hep. B Virus (HBV); blood born
  • Hep. C Virus (HCV); blood transfusion
  • Hep. D Virus (HDV); southeastern countries: water/food
  • Hep. E Virus (HEV); Southeastern countries: water/food
102
Q

Viral Hepatitis: Pathophysiology

A

Liver cells are damaged in two ways; direct action of virus or cell-mediated immune responses
Cell injury results in inflammation and necrosis in the liver
Hepatocytes and liver appear swollen and diffuse necrosis may be present

103
Q

Viral Hepatitis: Manifestations

A 
Range from mild or asymptomatic to severe
Course of hepatitis has 3 stages:
-Preicteric
-Icteric
-Posticteric
104
Q

Viral Hepatitis: Preicteric Stage

A

Onset may be insidious, with fatigue, malaise, anorexia, nausea and general muscle aching (feels like they have the flu; contagious)
Sometimes fever, headache, distaste for cigarettes, mild RUQ discomfort
Serum AST or ALT are elevated

105
Q

Viral Hepatitis: Icteric Stage

A

Onset of jaundice as serum bilirubin rises
As biliary obstruction increases stools lighten (clay-coloured), urine darkens (yellow/orange) and skin becomes pruritus
Liver tender and enlarged (hepatomegaly; able to palpate) and mild aching pain (more consistent)
Severe cases blood clotting factors impaired

106
Q

Viral Hepatitis: Posticteric Stage

A

Marked by reduction in signs, may extend over some weeks
Acute stage of hepatitis A lasts 8-10 weeks
Hepatitis B prolonged to 16 weeks (will be left a carrier for Hep. B

107
Q

Toxic or Nonviral Hepatitis

A

Hepatotoxins, such as chemicals or drugs, may cause inflammation and necrosis in the liver
May be due to direct effects of toxins or an immune response (hypersensitivity)
Toxic effects may be from sudden exposure or longterm (depending on severity, may require transplant)

108
Q

Hepatitis: Diagnostic Tests

A

Antibodies and antigens by serology
HbsAg- active or chronic carrier (infectious)
Anti HCV & HBV DNA (hep C infectious)
Prothrombin time - prolonged (liver plays key role in clotting)
WBC elevated
Liver biopsy if chronic hepatitis is suspected

109
Q

Gallbladder Disorders

A

Cholelithiasis: formation of gallstones which are masses of solid material or calculi that form in the bile
Cholecystitis: inflammation of gallbladder and cystic duct
Cholangitis: inflammation usually r/t infection of bile ducts
Choledocholithiasis: pertains to obstruction caused by gallstones of biliary tract

110
Q

Cholelithiasis: Gallstones

A

10% of population have them
Vary in size and shape
Increased risk after 40 years old, female, obese

111
Q

Cholelithiasis: Etiology

A

Small stones can pass silently
Lrg stones can obstruct flow of bile in cystic or common bile ducts
Can cause irritation and inflammation in gallbladder wall (cholecystitis) and tissue can then become infected
Gallstones from when bile contains inc. level of cholesterol or a deficit of bile salts

112
Q

Cholelithiasis: Etiology

A

Cholesterol gallstones occurs twice as often in women
High cholesterol levels in bile
Factors: obesity; high cholesterol intake; multiparty; medications

113
Q

Cholelithiasis: Etiology

A

Bile gallstones:

  • hemolytic anemia
  • Alcoholic cirrhosis
  • Biliary tract infection
114
Q

Cholelithiasis: Complications

A

Liver damage d/t back flow of bile
Pancreatitis d/t obstruction of common bile duct
Cholecystitis= inc. pressure = necrosis = inc. risk for perforation = peritonitis

115
Q

Cholelithiasis: Diagnostic Tests

A

Abd. U/S of RUQ
Oral cholecytogram
Gallbladder scan
Blod work (WBC, serum bilirubin, alkaline phosphate, ALT, AST)
ERCP - endoscopic retrograde cholangiopancreatography (can be diagnostic or treatment)

116
Q

Pancreatitis: Pathophysiology

A

Inflammation of pancreas resulting from auto digestion of the tissues
Autodigestion follows premature activation of pancreatic proenzymes within the pancreas (trypsin)
Digest the pancreatic tissue and cause massive inflammation, bleeding and necrosis

117
Q

Pancreatitis

A

Lipase causes fat necrosis
Blood vessels eroded by elastase (a protease) leading to hemorrhage
Cytokines and prostaglandins released and lead to widespread inflammation of peritoneal membrane (chemical peritonitis)
Increased capillary permeability - hpovolemia

118
Q

Pancreatitis: S&S

A

Sudden onset of acute pancreatitis may follow large meal or large amount of alcohol
Primary symptom: Severe epigastric pain or abd. pain radiating to back
Signs of shock: dec. BP, pallor, sweating and rapid weak pulse d/t inflammation, hemorrhage and therefore can lead to hypovolemia

119
Q

Pancreatitis: S&S

A

Low-grade fever until infection develops
Abd. distention, dec. bowel sounds, dec. peristalsis and paralytic ileum
Ecchymosis - flank (Turner’s sign) or umbilicus (Cullen’s sign) indicates severe hemorrhagic pancreatitis
Jaundice
N&V
Mental confusion/ agitation (hypoxic; respiratory distress)
Possible hyperglycemia

120
Q

Pancreatitis: Diagnostic Tests

A

Serum amylase inc. 12-24 hrs and dec. after 48
Serum lipase elevated and remain for weeks
Hypocalcemia (tetany) calcium binds to fatty acids in areas of necrosis
Urinary amylase - 24 hour urine collection can last up to 2 weeks

121
Q

Pancreatitis: Diagnostic Tests

A

CT scan
Endoscopic retrograde cholangiopancreatography (ERCP)
Ultrasonography/ x-ray

122
Q

Cirrhosis: Pathophysiology

A

Progressive disorder - liver failure
Extensive diffuse fibrosis and loss of lobular organization of the liver
Nodules of regenerated hepatocytes may form but are nonfunctional
Impaired blood flow thru liver increases pressure in portal venous system

123
Q

Cirrhosis: Causes

A 
Congenital (Cystic Fibrosis)
Inherited metabolic disorders
Long-term exposure to toxins
Chronic alcoholics
Hepatitis positive
124
Q

Cirrhosis: Classified by structural changes

A

Alcoholic liver disease (portal cirrhosis)
Biliary cirrhosis
Postnecrotic cirrhosis

125
Q

Cirrhosis: Alcoholic liver disease

A 
Several stages  of development
Alcohol metabolites
Malnutrition
Initial - Accumulation fat in liver cells
- Enlargement of liver (hepatomegaly)
- Reversible if alcohol intake reduced
126
Q

Cirrhosis: Second and Third Stage

A 
Second Stage:
Alcoholic hepatitis
Inflammation and cell necrosis
Fibrous tissue forms - irreversible
Third Stage:
End-stage cirrhosis (complete and irreversible liver failure)
Fibrotic tissue replaces normal tissue
Significant altering liver structure
127
Q

Cirrhosis: Biliary cirrhosis

A

Immune disorder
Obstruction of bile flow due to stones or mucous plugs
Inflammation, necrosis and fibrosis

128
Q

Cirrhosis: Posstnecrotic cirrhosis

A

Linked chronic hepatitis
Exposure to toxic materials
(Tylenol, Wilson’s disease, neoplasms (cancer))

129
Q

Cirrhosis: Effects of

A

Effects of cirrhosis evolve from two factors:
Loss of liver cell function
Interference with blood and bile flow in liver

130
Q

Cirrhosis: Major functional losses

A

Dec. removal and conjugation of bilirubin
Dec. production of bile
Impaired digestion and absorption of nutrients
Dec. production blood-clotting factors (VK+ is essential)
Impaired glucose and glycogen metabolism

131
Q

Cirrhosis: Obstruction of blood and bile

A 
Dec. amount of bile entering intestines
Impaired digestion and absorption
Backup bile in liver - jaundice
Blockage of blood flow - portal hypertension
Congestion in spleen - splenomegaly
132
Q

Cirrhosis: Manifestations

A 
Fatigue, anorexia, indigestion, wt loss
Dull aching pain RUQ
Ascites (fluid in stomach)
General edema
Esophageal varices
Splenomegaly
Anemia
133
Q

Complications of Cirrhosis

A 
Portal hypertension
Ascites
Bleeding esophageal varices
Coagulation defects
Jaundice
Hepatic encephalopathy with hepatic coma
Hepatorenal syndrome
134
Q

Port Hypertension

A

Sluggish blood flow resulting in increased pressure in portal circulation
Congested venous drainage of the GI tract

135
Q

Portal Hypertension: Manifestations

A

Anorexia
Varices (esophageal, gastric, hemorrhoidal) can rupture; cause uncontrolled bleeding
Ascites

136
Q

Esophageal Varices

A 
Results from portal hypertension
Alcoholic or posthepatic cirrhosis
Infection from liver flukes
Vasoactive hormones
Increased splanchnic blood flow
Increased vascular resistance in the liver
137
Q

Esophageal Varices: Manifestations

A 
Hematemesis (vomiting blood)
Melena (passage of dark, pitchy, and grumous stools stained with blood pigments)
Bright red rectal bleeding
Anemia
Shock
138
Q

Hepatic Encephalopathy

A

Complex neuropsychiatric syndrome from too much ammonia

Associated with hepatic failure or severe chronic liver disease

139
Q

Hepatic Encephalopathy: Manifestations

A 
Psychotic symptoms
Spastic myelopathy
Cerebellar/ extrapyramidal signs
Asterixis "liver flap" (classic sign)
- Spastic jerking of hands held in forced extension
Dementia
140
Q

Hepatorenal Syndrome

A

Acute and progressive disease
Normal kidney with disturbed infrarenal blood flow
- Related to imbalance between vasoconstriction and vasodilating mechanisms
Rising serum creatinine levels and oliguria

141
Q

Cirrhosis: Diagnostic Tests

A

Liver biopsy; determine cause and extent of damage
Chemistry; CBC, electrolytes, amino acids, ammonia, LFT’s
Coagulation studies; risk of bleeding
Abdominal ultrasounds; liver size, nodules, ascites
Upper endoscopy; esophageal varices

Patho II (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions